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Magnetic resonance imaging spectrum of perinatal hypoxic-ischemic brain injury

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ABSTRACT

Perinatal hypoxic–ischemic brain injury results in neonatal hypoxic–ischemic encephalopathy and serious long-term neurodevelopmental sequelae. Magnetic resonance imaging (MRI) of the brain is an ideal and safe imaging modality for suspected hypoxic–ischemic injury. The pattern of injury depends on brain maturity at the time of insult, severity of hypotension, and duration of insult. Time of imaging after the insult influences the imaging findings. Mild to moderate hypoperfusion results in germinal matrix hemorrhages and periventricular leukomalacia in preterm neonates and parasagittal watershed territory infarcts in full-term neonates. Severe insult preferentially damages the deep gray matter in both term and preterm infants. However, associated frequent perirolandic injury is seen in term neonates. MRI is useful in establishing the clinical diagnosis, assessing the severity of injury, and thereby prognosticating the outcome. Familiarity with imaging spectrum and insight into factors affecting the injury will enlighten the radiologist to provide an appropriate diagnosis.

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A 29-day-old term neonate, with severe hypoxic ischemic encephalopathy (stage III) at birth, shows basal ganglia thalamic pattern of injury. (A, B) Axial T1WI at the level of lateral and third ventricles show hyperintensity at the bilateral ventrolateral thalami and posterior putamina, and T1 hypointensity (cyst) at left globus pallidus. Also note the nonvisualization of myelination (T1 hyperintensity) at the posterior limb of internal capsule. Axial FLAIR (C) and (D) T2WI at the level of lateral ventricles show cerebrospinal fluid (CSF) intensity cyst (T2 hyperintensity and suppression of signals on FLAIR) with peripheral gliosis at the left globus pallidus. Note the subtle T2 hyperintensity at the bilateral posterior putamina and ventrolateral thalami and the minimal cystic changes at the bilateral frontal periventricular white matter
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Figure 11: A 29-day-old term neonate, with severe hypoxic ischemic encephalopathy (stage III) at birth, shows basal ganglia thalamic pattern of injury. (A, B) Axial T1WI at the level of lateral and third ventricles show hyperintensity at the bilateral ventrolateral thalami and posterior putamina, and T1 hypointensity (cyst) at left globus pallidus. Also note the nonvisualization of myelination (T1 hyperintensity) at the posterior limb of internal capsule. Axial FLAIR (C) and (D) T2WI at the level of lateral ventricles show cerebrospinal fluid (CSF) intensity cyst (T2 hyperintensity and suppression of signals on FLAIR) with peripheral gliosis at the left globus pallidus. Note the subtle T2 hyperintensity at the bilateral posterior putamina and ventrolateral thalami and the minimal cystic changes at the bilateral frontal periventricular white matter

Mentions: This pattern of injury is usually seen following an acute sentinel event such as ruptured uterus, placental abruption, or cord prolapse. Hence, this is also referred as a pattern following “acute near severe asphyxia.” Because the injury primarily involves the bilateral ventrolateral thalami and posterior putamina, it is also known as basal ganglia–thalamus pattern (BGT) [Figure 11].


Magnetic resonance imaging spectrum of perinatal hypoxic-ischemic brain injury
A 29-day-old term neonate, with severe hypoxic ischemic encephalopathy (stage III) at birth, shows basal ganglia thalamic pattern of injury. (A, B) Axial T1WI at the level of lateral and third ventricles show hyperintensity at the bilateral ventrolateral thalami and posterior putamina, and T1 hypointensity (cyst) at left globus pallidus. Also note the nonvisualization of myelination (T1 hyperintensity) at the posterior limb of internal capsule. Axial FLAIR (C) and (D) T2WI at the level of lateral ventricles show cerebrospinal fluid (CSF) intensity cyst (T2 hyperintensity and suppression of signals on FLAIR) with peripheral gliosis at the left globus pallidus. Note the subtle T2 hyperintensity at the bilateral posterior putamina and ventrolateral thalami and the minimal cystic changes at the bilateral frontal periventricular white matter
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC5036328&req=5

Figure 11: A 29-day-old term neonate, with severe hypoxic ischemic encephalopathy (stage III) at birth, shows basal ganglia thalamic pattern of injury. (A, B) Axial T1WI at the level of lateral and third ventricles show hyperintensity at the bilateral ventrolateral thalami and posterior putamina, and T1 hypointensity (cyst) at left globus pallidus. Also note the nonvisualization of myelination (T1 hyperintensity) at the posterior limb of internal capsule. Axial FLAIR (C) and (D) T2WI at the level of lateral ventricles show cerebrospinal fluid (CSF) intensity cyst (T2 hyperintensity and suppression of signals on FLAIR) with peripheral gliosis at the left globus pallidus. Note the subtle T2 hyperintensity at the bilateral posterior putamina and ventrolateral thalami and the minimal cystic changes at the bilateral frontal periventricular white matter
Mentions: This pattern of injury is usually seen following an acute sentinel event such as ruptured uterus, placental abruption, or cord prolapse. Hence, this is also referred as a pattern following “acute near severe asphyxia.” Because the injury primarily involves the bilateral ventrolateral thalami and posterior putamina, it is also known as basal ganglia–thalamus pattern (BGT) [Figure 11].

View Article: PubMed Central - PubMed

ABSTRACT

Perinatal hypoxic–ischemic brain injury results in neonatal hypoxic–ischemic encephalopathy and serious long-term neurodevelopmental sequelae. Magnetic resonance imaging (MRI) of the brain is an ideal and safe imaging modality for suspected hypoxic–ischemic injury. The pattern of injury depends on brain maturity at the time of insult, severity of hypotension, and duration of insult. Time of imaging after the insult influences the imaging findings. Mild to moderate hypoperfusion results in germinal matrix hemorrhages and periventricular leukomalacia in preterm neonates and parasagittal watershed territory infarcts in full-term neonates. Severe insult preferentially damages the deep gray matter in both term and preterm infants. However, associated frequent perirolandic injury is seen in term neonates. MRI is useful in establishing the clinical diagnosis, assessing the severity of injury, and thereby prognosticating the outcome. Familiarity with imaging spectrum and insight into factors affecting the injury will enlighten the radiologist to provide an appropriate diagnosis.

No MeSH data available.


Related in: MedlinePlus